The mechanisms responsible for persistent slow growth in fetal alcohol syndrome (FAS) are not understood. We hypothesize that the poor growth is a result of identificable endocrine abnormalities or abnormal tissue response to endocrine factors. FAS children, their normal siblings, and short controls will be evaluated with regard to overnight GH, GH stimulation and IGF-1 generation by exogenous GH. Subsequent in vitro study and treatment protocols will depend on results of this initial work.